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Life
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Molecular Mechanisms in Pain Signaling Pathways
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Molecular Mechanisms in Pain Signaling Pathways

A special issue of Life (ISSN 2075-1729). This special issue belongs to the section "Physiology and Pathology".

Deadline for manuscript submissions: closed (30 November 2023) | Viewed by 3975

Special Issue Editors

Dr. Boris Krylov

E-Mail Website
Guest Editor
Head of the Laboratory of Physiology of Excitable Membranes, Pavlov Institute of Physiology of the Russian Academy of Sciences, 199034 Saint Petersburg, Russia
Interests: nociception; sensory neurons; Na,K-ATPase as a signal transducer; Nav1.8 sodium channels
Dr. Ke Ma

E-Mail Website
Guest Editor
Medicine School, Shanghai Jiaotong University, Shanghai 200240, China
Interests: neuropathic pain; sympathetic nerve; sodium channel; opioid tolerance; interventional treatment

Special Issue Information

Dear Colleagues,

The medicinal treatment of chronic pain of various etiologies requires the use of opiates and/or opioids, which evoke adverse side effects at the organismal level and are highly addictive. For this reason, the world is experiencing an opioid crisis, representing one of the worst public health crises in history. When pain as a sensation loses its informational and protective function and becomes chronic, this pathology can be corrected only by drug administration. Regretfully, there are no safe and effective analgesics that can replace opiates in the arsenal of clinical medicine.

А possible approach to help solve this challenging problem is to modulate the functional activity of ion channels encoding the nociceptive information. It is the high-frequency component of impulse firing that carries information about the pain sensation to the CNS. The desire to specifically eliminate this high-frequency impulse activity component of polymodal nociceptors, leaving the signals of other modalities intact, forces us to look for novel approaches to the creation of fundamentally new, effective, and safe drugs that can replace opiates and opioids in clinical practice.

Dr. Boris Krylov
Dr. Ke Ma
Guest Editors

Manuscript Submission Information

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Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • nociception
  • impulse firing
  • ion channels
  • Na,K-ATPase as a signal transducer

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Published Papers (2 papers)

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Research

12 pages, 1225 KiB  
Article
Clinical Biomarker of Sterile Inflammation, HMGB1, in Patients with Chronic Non-Specific Low Back Pain: A Pilot Cross-Sectional Study
by Julita A. Teodorczyk-Injeyan, Heba Khella and H. Stephen Injeyan
Life 2023, 13(2), 468; https://doi.org/10.3390/life13020468 - 8 Feb 2023
Viewed by 1577
Abstract
The present study explores whether the inflammatory biomarker of sterile inflammation, high mobility box 1 (HMGB1), contributes to the inflammatory/nociceptive pathophysiology that characterizes chronic non-specific low back pain (LBP). Patients with chronic LBP (N = 10, >3 pain score on a 11-point Visual [...] Read more.
The present study explores whether the inflammatory biomarker of sterile inflammation, high mobility box 1 (HMGB1), contributes to the inflammatory/nociceptive pathophysiology that characterizes chronic non-specific low back pain (LBP). Patients with chronic LBP (N = 10, >3 pain score on a 11-point Visual Analogue Scale, VAS) and asymptomatic participants (N = 12) provided peripheral blood (PB) samples. The proportion of classical CD14++ monocytes within PB leukocytes was determined by flow cytometry. The plasma and extracellular HMGB1 levels in unstimulated adherent cell (AC) cultures were measured using specific immunoassays. HMGB1 localization in ACs was assessed by immunofluorescent staining. The relative gene expression levels of tumor necrosis factor α (TNFα), interleukin-1 beta (IL-1β) and HMGB1 were determined by quantitative polymerase chain reaction (qRT-PCR) in relation to the pain intensity (11-point VAS scores) in patients with LBP. The extracellular release of HMGB1 in the LBP patient AC cultures was significantly elevated (p = 0.001) and accompanied by its relocation into the cytoplasm from the nuclei. The number of CD14++ monocytes in the patients’ PB was significantly (p = 0.03) reduced, while the HMGB1 plasma levels remained comparable to those of the controls. The mRNA levels of TNFα, IL-1β and HMGB1 were overexpressed relative to the controls and those of HMGB1 and IL-1β were correlated with the VAS scores at a significant level (p = 0.01–0.03). The results suggest that HMGB1 may play an important role in the pathophysiology of chronic non-specific LBP. Full article
(This article belongs to the Special Issue Molecular Mechanisms in Pain Signaling Pathways)
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14 pages, 3606 KiB  
Article
Role of Transient Receptor Potential Vanilloid 1 in Sonic Hedgehog-Dependent Taste Bud Differentiation
by Yun-Hee Rhee, Young-Hoon Choi, Allison C. Hu, Min Young Lee, Jin-Chul Ahn, Sehwan Kim, Ji-Hun Mo, Seung Hoon Woo and Phil-Sang Chung
Life 2023, 13(1), 75; https://doi.org/10.3390/life13010075 - 27 Dec 2022
Cited by 1 | Viewed by 1663
Abstract
Taste bud cell differentiation is extremely important for taste sensation. Immature taste bud cells cannot function during taste perception transmission to the nerve. In this study, we investigated whether hedgehog signaling affected taste bud cell differentiation and whether transient receptor potential vanilloid 1 [...] Read more.
Taste bud cell differentiation is extremely important for taste sensation. Immature taste bud cells cannot function during taste perception transmission to the nerve. In this study, we investigated whether hedgehog signaling affected taste bud cell differentiation and whether transient receptor potential vanilloid 1 (TRPV1) played a key role in dry mouth. The induction of dry mouth due to salivary gland resection (SGR) was confirmed on the basis of reduced salivation and disrupted fungiform papillae. The expression of keratin 8 (K8) of taste bud cells, neurofilament (NF), sonic hedgehog (Shh), and glioma-associated oncogene homolog 1 (Gli1) around taste bud cells was downregulated; however, the expression of TRPV1, P2X purinoceptor 3 (P2X3), and hematopoietic stem cell factor (c-Kit) was upregulated at the NF ends in the dry mouth group. To investigate the effect of TRPV1 defect on dry mouth, we induced dry mouth in the TRPV-/- group. The K8, NF, and P2X3 expression patterns were the same in the TRPV1 wild-type and TRPV1-/- dry mouth groups. However, Shh and c-Kit expression decreased regardless of dry mouth in the case of TRPV1 deficiency. These results indicated that TRPV1 positively regulated proliferation during taste bud cell injury by blocking the Shh/Gli1 pathway. In addition, not only cell proliferation but also differentiation of taste bud cells could not be regulated under TRPV1-deficiency conditions. Thus, TRPV1 positively regulates taste bud cell innervation and differentiation; this finding could be valuable in the clinical treatment of dry mouth-related taste dysfunction. Full article
(This article belongs to the Special Issue Molecular Mechanisms in Pain Signaling Pathways)
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